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Pre-084

cr00k, you have blasphemed.

S-iso is my child. It is all that I love. It comes around every month or so, and it is a blessing to me. I am a K-head. S-Ketamine is my favourite drug. I use it sparingly. It is my master. It is beautiful, it is sublime.

If it has not shown you the glory, then you may be getting the sub-standard stuff. I'm a disso person, I'm a K-head but just enough for it to be a treat. I love ACH's and all that surrounds them. I am a connoisseur of dissociatives and want to get right into the heart of NMDA antagonists. If you do not share this love then let bygones be bygones.

Psychedelics, of course, are the main goal of my endeavors but dissos give the power to work and be happy doing it. There may be adverse reactions to them but ultimately they should be produced as a way of life. The compounds in this field are too important to just be laid to rest.

I'm loving these conversations with you but you really, truly need to see the side I have seen in S(+) Ketamine. It's just the tits! I suppose other people have different ideas and feelings about drugs but S-K turned my life around. We may have differences of viewpoints but I will not let it stand between us. I guess it's like Marmite!

To be honest if you loved it, it'd probably work out worse than it is now. We all have our own vices, mine is Ketamine (s-ketamine), yours is...what is your DOC? But let us not argue over how one compound works with one as opposed to another. I'm here for the exploration and I gather you are too, so lets explore together.

I have to say the pivotal point in my drug career was with Inresa Ketamine. It was truly the greatest drug experience of my life, it was racemic and it was German, so all my gratitudes go to your home country. It was amazing and I don't think anything will top that. Even my most recent +4, with DOET, cannot stand up to the magic I saw in that Inresa hole. I think there may be a slight aversion to the racemic claims they show, perhaps 60:40 with the S+ holding the majority. It certainly was fluffy, indicating positive ions and I butchered that bag while watching 'Trance' by Danny Boyle. It was absolute perfection.

Oh and the other day, I had some s-iso K and railed the better part of a gram while watching Apocalypse Now. It was incredible!
 
blueberries said:
Yeah, you're both right. I don't think it produced any change. At the time I was in a bit of a placebo mode and the 3-MeO was a little overwhelming, which goaded me into thinking there was an alteration. I'll try again but with a larger dose of Lamictal. If the IC50 is 145uM then to get to an adequate level you'd need to use say 5x as much to get to a space where the Lamictal would have an affect on the 3-MeO-PCP, who's binding affinity to s1 is around 42nM. So they'd both be around the 30-40nM level. My one concern is due to the horror stories of people taking too much Lamicatal and gaining temporary epilepsy (or consistent epilepsy as in some cases). I think that's just after continued use over a period of several months/years the suddenly dropping it, so I should be ok.
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You're going from nM to uM, so you actually need about 5000x as much lamictal as 3-MeO, assuming equivalent oral bioavailability and what not.
 
endotropic said:
You're going from nM to uM, so you actually need about 5000x as much lamictal as 3-MeO, assuming equivalent oral bioavailability and what not.
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Yes, for a 10 mg dose of 3-meo-pcp that would mean taking 50000 mg or 50 g of Lamictal.

The strongest Lactimal tablets contain 200 mg, but even then you would have to take 250 tablets. ;)
 
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Yeah I realised that soon after I posted it. I was going to edit it but I had to run out to get something.
 
Ha, don't get me wrong here I've been a huge fan of ketamine and other dissociatives for ten years now. I love ketamine. I think it's pretty obvious that someone who iv's 160mg racemic k without a tolerance has to love the stuff. I just don't understand why you prefer the s isomer over the racemic k because the s simply isn't as psychedelic for most people, including me. That is why it was introduced to the market in the first place.
I IV ketamine precisely because it brings out the psychedelic effects much better compared to insufflating it or taking it orally/rectally. Even IV'ed s isomer never is as psychedelic as the corresponding insufflated dose of racemic ketamine in my experience. All the effects I seek aren't as pronounced with it, most of all the propioceptive pseudohallucinations and the CEVs. Could you elaborate what you find in it that racemic ketamine can't offer?

I hope you adjust your dosages accordingly because the s isomer is a lot stronger than the r isomer (and therefore considerably stronger than the racemic as well, about 1:1.5).

Racemic ketamine should always be 50:50, give or take a few molecules. Different r/s ratios have of course been used in studies, but I don't think there are any pharmaceutical products out there that aren't either racemic or mostly s isomer. Btw I don't think I've ever had cut ketamine, unless you consider the NaCl in "dried" ketamine a cutting agent.^^
That stuff used to be so cheap and no one ever wanted it. Some dealers were handing it out for free because there was no market for it at all. I once traded 100g pharmaceutical ketamine for some blotter that had cost me 30 Euros lol. Now everyone and his dog (pun intended) knows about it. It's highly sought after these days, there's never enough to satisfy the demand it seems and prices for crystalline ketamine range from 30 to 50 Euros for consumers down here, regardless of isomer.

Regarding my drug of choice, I don't think I've ever been as fond of a drug as I am of ketamine except maybe of DMT and PCP, not counting cannabis. Tramadol also ranks very high up there for me, higher than any other "opiate" (though it really isn't one).

This is seriously OT... Sorry guys.
 
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Ok, so I was going to post this (see below) but then I looked into it further and now I'm really not sure about anything. You see I've always had a much fuller psychedelic experience from S(+) Ketamine but this thread is suggesting the opposite (however subjectively). It could be that people are misinterpreting deleriant or k opioid type effects with psychedelic effects, which in my mind means only HT2a mediated processes (AKA: lots of colour and 'proper' visuals). So the question is if the R(-) isomer produces more deleriant effects does the S(+) isomer produce HT2a agonism along with a tighter binding to NMDA? This would produce more psychedelic effects but a completely different kind of hallucinogenic experience from the R(-) isomer.

I think I need to take another closer look at racemic K as I primarily use S(+) Ketamine, however a couple of weeks back I did have some racemic which I holed on (nothing special though) but my most recent experience was with S(+), which I used solely for it's euphoric properties (which would indicate a higher level of dopamine reuptake inhibition as stated in the thread). I also really want to try some R(-) now too, but it's just so rare these days.

In all honesty I'll probably stick to S(+) just because it's more potent but if some non-Indian K comes around, I'll be using that instead as Indian is usually fairly impure.

It really is OT but I'm glad to hear you're a k-head too! Bringing it back around S(+) K seems to have less sigma agonism than R(-) K. I also got hold of a paper which suggested sigma1 agonism inhibited glutamatergic processes and NMDA activity http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2596726/#R10. Though racemic would inhibit NMDA less than S+ which is correlated in this thread: http://www.bluelight.org/vb/threads/447697-Ketamine-Subthread-Isomers-R-and-S-Ketamine

However the thread also suggested S(+) isomer K to antagonise NMDA moreso than R(-), which would indicate a higher level of psychotomimetic activity. Hence the S(+) isomer would be more 'psychedelic' as I have personally found. There is a great deal less inhibition of motor function in S but more of the wall collapsing and turning into an Escher dreamscape. The paper goes on to describe how (+) Pentazocine has a relatively high degree of sigma1 activity at high doses therefore inhibiting NMDA activity, producing more psychotomimetic reactions. However Pentazocine is a well known k opioid agonist so it's psychotomimetic effects would be based upon that mechanism much more than NMDA antagonism.

So sigma inhibits NMDA producing more psychedelic effects but S(+) K inhibits NMDA 3-4 times more than R(-) suggesting it's psychedelic effects come mostly from sigma agonism rather than purely NMDA antagonism, which would in turn produce more anaesthetic action than R(-). So on the 'hole' (pun intended) S(+) would give more sedation and more psychedelic affect than R(-). As of yet though, I have never tasted R(-) Ketamine so I cannot comment on it subjectively, although I'd love to get my hands on some.

Also another reason for my love of S(+) is the lower dose, as my tolerance is relatively high and racemic just doesn't do it for me any more, unless I go for ridiculessly high doses.
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EDIT: Again sorry for going off topic but we should discuss sigma along with our mini discussion about K too.
 
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So did he take the drugs?? THIS STORY NEEDS CLOSURE
 
sekio said:
As judged by what? Some guy with no analytical tools? :p
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Probably judged by color? That's one of the properties which can hint at the degree of purity and do not necessarily require equipment (like a spectrometer in this case). Melting point can also be tested with a thermometer alone. Agreed though, people who judge the purity of a substance usually do so by looking at how smashed they get which is influenced by too many other factors and variance between individuals to be of any relevance.

I never noticed any difference between crystalline ketamine that was from India, Pakistan, China, SE Asia, Germany or dried from vials. There's obviously a big difference between the 2 isomers (with 50r/50s=racemic and s isomer usually being available), but other than that I've never noticed any difference between the ketamine batches I've sampled. I might just not appreciate subtle differences, bit I sure the fuck have sampled a lot of ketamine. ;)
 
Judging purity by color isn't even that useful, you can have impurities as low as 0.01% effect the color of the resulting crystals/solution. Likewise you can have colorless impurities.
 
sekio said:
Judging purity by color isn't even that useful, you can have impurities as low as 0.01% effect the color of the resulting crystals/solution. Likewise you can have colorless impurities.
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Yeah good point.
 
Bumping this thread as it's available again.
 
Unrelated to this compound specifically. But I've noticed interesting results from administering 3-meo-pcp (high affinity ligand for σ-2 receptor and obviously a selective NMDA antagonist, without evidence of off-target action at dopamine or serotonin receptors) alongside noopept/fasoracetam/sunifiram.

My experience when using any of those to "sober up" from MXE has always been that 2 + -2 doesn't exactly equal 0. But with 3-meo-pcp, the inebriating effect does seem to be much more "cleanly" abolished--though perhaps leaving a tad of its "manic" nature intact. Obviously, AMPA agonism and sub-unit selective NMDA agonism doesn't *precisely* cancel out PCP-site NMDA antagonism, but it comes close enough to doing so that this is probably the most accessible method of approximating selective σ-receptor stimulation.

3-meo-pcp only hits the one σ subtype, however. 3-meo-pce seems to hit both equally, so perhaps that would be a better compound to test subjective σ activity with.
 
No idea if PRE-084 gets clinical trials in humans but I hope that in stage III it gets checked against ketamine as an anti-depressant considering that AD effect is thought to be related to effects in neuroplasticity - so the AD-like action suggested for PRE-084 may work that same way?
Can drugs like noopept, selank or semax also have that AD potential? I'm interested in whether / when we can answer what the conditions are for neurotrophic involvement leading to anti-depressant potential.

If it's only BDNF, not GDNF that can be 'utilized' that way, any AD action of PRE-084 would seem only a result of the sigma activity. I'd personally not experiment with this until there is a lot more clarified about sigma 1 vs. sigma 2 and tweaking the action selecting one or the other subtype with agonists or antagonists. Anti-depressant action, but also anti-psychotic or psychomimetic?, convulsant? What a crapshoot, and any of these may even prove to be even misidentified in this preliminary stage when concluded from drug research with compounds that are not selective?!
 
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Snorting is painful.

It's not very active on its own. Up to 10mg showed not many effects. I feel a bit more alert and clear headed, but no recreational high to speak of.

Few minutes later: I'm totally not a morning person at all, however I feel somewhat awake and stimulated and am multitasking a few things at once. So there's definitely something going on. No euphoria to speak of though.

I'll try other ROAs and mixing it with some other stuff!
 
22 mg PRE-084 taken sublingually this morning, along with my morning caffeine and Kratom. Good focus and chipper mood. 1 hour later, I feel very well, have a good appetite and am about to tackle my day's work. Very unscientific, but I am happy to oblige anyones curiosity.
 
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